Title: Dementias
1Dementias
- As of 4Feb2015. All items from DSM-IV, DSM-5, APA
Practice Guidelines, Taman/Mohr Text, or
Sadock/Sadock/Ruiz Text unless otherwise
indicated.
2Dx criteria
- Q. What is the outline of the DSM dx criteria of
dementia?
3Dx criteria - general
- Ans.
- 1. Multiple cognitive deficits.
- 2. Gradual onset and decline
- 3. Not part of another Disorder
4Dx criteria Specific Cognitive deficits
- Q. What cognitive deficits are part of the DSM
criteria of dementia?
5Dx specific cognitive deficits
- Ans.
- 1. Memory impairment
- AND
- 2. At least one of the following
- Aphasia
- Apraxia
- Agnosia
- Executive functioning deficits
-
6Early onset
- Q. What is the dividing line between early and
late onset dementia?
7Early Onset
- Ans.
- lt or 65, early onset
- gt 65, late onset
8Reasons to hospitalize
- Q. List reasons to hospitalize pts with dementia.
9Reasons to hospitalize
- Ans.
- 1. Symptom severity
- Dangerousness to self or others, including
inability of caretakers to care for the pt - 2. Intensity of care and treatment needed
- -- evaluations or treatments that cannot by done
on outpt basis.
10Follow-up
- Q. If you have a routine pt with Alzheimers,
how often should the pt be monitored by you?
11Follow-up
- Ans. Every 3 to 6 months.
12MMSE
- Q. What is the MMSE? And What does it evaluate?
13MMSE
- Ans.
- MMSE Mini-mental status examination.
- MMSE tests cognitive functioning.
14CT or MRI
- Q. When is CT or MRI advised as part of the
initial eval of people with dementia?
15CT or MRI
- Ans. Some would say in all, but the question is
more likely to focus on when one of these tests
is more indicated than most pts with dementia - Early onset
- Relatively rapid onset
- High vascular risk factors suggested
- Neurological exam suggests local lesions
16Neuropsych testing
- Q. When is neuropsych testing indicated?
17Neuropsych testing
- Ans. When questions arise as to whether the
individual actually has a dementia. - Keep in mind that only Mental Retardation and
Learning Disorders has psychological testing as
part of a DSM criteria set.
18Gene testing
- Q. Is gene testing recommended?
19Gene testing
- Ans. Gene testing is not recommended. Dx is
clinically based regardless of genes. See
exceptions infra
20Apolipoprotein E-4
- Q. What is the significance of apolipoprotein E-4
(APOE-4)?
21Apolipoprotein E-4
- Ans. Apolipoprotein E-4 APOE-4, on chromosome
19, is more common in individuals with
Alzheimers but not diagnostic.
22Suicidal
- Q. At what stage of a dementia is suicidal
ideation most common?
23Suicidal
- Ans. Most common when the disease is still mild.
24Suicide and gender
- Q. Which gender is suicide most common in this
illness?
25Suicide and gender
- Ans. Men
- In answering exam questions as to successful
suicides, keep in mind that men do so far more
often than women, and that is even more true in
the elderly.
26Falls
- Q. Give one of major ways a physician can reduce
the chances of falls in pts with dementia.
27Falls
- Ans. Review and considered discontinuance of meds
associate with falls.
28Driving
- Q. Should a physician report their patient who
has dementia to the state department of motor
vehicles?
29Driving
- Ans. Varies by state. Required in some,
forbidden in others.
30Dosing in the elderly
- Q. What are the principles of medicating in the
elderly?
31Medicating the elderly
- Ans.
- -- lower starting doses.
- -- longer intervals between dose increases.
- -- smaller dose increase
32Medicating rules - why
- Q. Why the go-slow approach with the elderly?
33Medicating rules - why
- Ans.
- slower hepatic metabolism
- decreased renal clearance
34Goal of medicating
- Q. What is the goal of medicating a patient with
Alzheimers?
35Goal of medicating
- Ans. Delay progression of the disease. No med
reverses.
36FDA for Alzheimers
- Q. What meds have been approved for Alzheimers?
37FDA for Alzheimers
- Ans.
- donepezil
- galantamine
- memantine
- rivastigmine
- tacrine
38FDA med action
- Q. Which of the five is/are cholinesterase
inhibitors? Which is/are NMDA antagonist?
39Meds - actions
- Ans.
- donepezil, galantamine, rivastigmine, and
tacrine are cholinesterase inhibitors. - memantine is a noncompetitive N-methyl-aspartate
antagonist, glutamate antagonist.
40Vitamin E
- Q. What about high doses of Vitamin E for
Alzheimers?
41Vitamin E
- Ans. Not proven to be useful and high doses may
be associated with increased risk of heart
failure. - Vitamin E must be avoided in patients with
vitamin K deficiencies.
42Q. Selegiline
- 1 Selegilines usefulness in dementia?
- 2 Especially problematic?
43Ans. Selegiline
- 1 Not proven to be useful.
- 2 Should not be given to pt on an
antidepressant.
44Tacrine
45Tacrine
- Ans. Regarded as less preferred to donepezil,
rivestigmine, and galantamine because of
tacrines hepatic toxicity.
46ECT
- Q. Indications for ECT in pts with Alzheimers?
47ECT
- Ans. Indicated for pts with moderate to severe
depression and Alzheimers and who do not respond
to or cannot tolerate antidepressant meds.
48Delusions and hallucinations
- Q. Pt is moderately impaired from Alzheimers,
has delusions and hallucinations and is not
distressed or agitated, meds?
49Hallucinations and delusions
- Ans. No meds, instead reassurance, redirection
and distractions.
50Hallucinations and delusions
- Q. Alzheimers pt with hallucinations and
delusions and combative, meds?
51Hallucinations and delusions
- Ans. Low dose antipsychotic.
- This is true of the Guides. Recent FDA warnings
would suggest ordering antipsychotics at quite
low levels to begin -- given the increased death
rate of the elderly on antipsychotics.
52Profoundly impaired
- Q. What meds help the cognition of the severely
impaired?
53Profoundly impaired
- Ans. Memantine is approved for the profoundly
impaired. Cholinesterase inhibitors are not.
54Meds Delirium
- Q. What classes of meds can cause delirium in
those with Alzheimers?
55Delirium meds
- Ans. Virtually all psychotropic meds, even more
so, those having anticholinergic activity.
56Anticholinergic
- Q. What are some meds psychiatrists use that have
anticholinergic activity?
57Anticholinergic
- Ans. Tricyclics, low-potency antipsychotics, and
diphenhydramine.
58Dopaminergic meds
- Q. Dopaminergic meds used in Parkinsons disease
in pt who also has Alzheimers predisposes that
pt to?
59Dopaminergic meds
- Ans. Visual hallucinations
60Vascular dementia
- Q. Treatment for vascular dementia?
61Vascular dementia
- Ans.
- -- control BP
- -- low-dose aspirin
- 2 of 3 trials with donepezil found some positive
results, but the 3rd trial lack of effectiveness
probably precludes it being the correct answer.
62Fronto-temporal dementia
- Q. What med has been shown to decrease
problematic behaviors of fronto-temporal
dementia, e.g., agitation?
63Fronto-temporal dementia
- Ans. Trazodone.
- If trazodone is not one of the choices,
amantadine has some anecdotal support.
64Caregivers and depression
- Q. To what degree does depression occur in
caregivers?
65Caregivers and depression
- Ans.
- 30 of spousal care-givers experience a
depressive disorder. - 22-37 of adult children care-givers, the higher
percentage, gt 30, in those with a prior hx of a
mood disorder.
66Federal Regulation
- Q. A major law, passed in 1987, that regulates
the use of physical restraints and use of meds in
nursing home is?
67Federal Regulation
- Ans. The Omnibus Budget Reconciliation Act of
1987 OBRA.
68Gender
- Q. In Alzheimers, which gender is more frequent?
69Gender
- Ans. More common in women.
70African Americans
- Q. Relative to Caucasians, Which dementias do
African Americans have more and which do they
have less?
71African Americans
- Ans. More vascular dementia could guess from
their higher hypertension rate and less
Parkinsonian dementias.
72Family Hx
- Q. If Mrs. X has Alzheimers, what the chances of
her siblings or children getting Alzheimers?
73Family hx
- Ans. Two to four times that of the general
population.
74Genes early onset
- Q. What are the three genes that have an
increased association with early on-set
Alzheimers?
75Genes early onset
- Ans.
- 1. Amyloid precursor protein APP on chromosome
21 - 2. Presenilin 1 PSEN1 on chromosome 14
- 3. Presenilin 2 PSEN2 on chromosome 1
76Vascular dementia
- Q. Onset and course of vascular dementia?
77Vascular dementia
- Ans. Acute onset and step-wise decline.
78Alzheimers onset - age
- Q. Give the approximate onset of Alzheimers per
the age of the individual, such as per year of - lt 65
- 65-70
- 70-75
- 75-80
- 80-85
- gt85
79Alzheimers onset - age
- lt 65 rare
- 65-70 0.5/ year i.e., one in 200 will develop
Alzheimers within a year - 70-75 1
- 75-80 2
- 80-85 3
- gt85 8 Means that the odds of someone who does
not have Alzheimers at 85 has an 8 chance of
having the onset over the next 12 months. The
jump from 3 to 8 doesnt seem correct for 85
y/o compared to 84 y/o, so the 8 percent must
be based on the average of all over 85. Im not
sure.
80Mild cognitive impairment
- Q. Criteria for mild cognitive impairment?
81Mild cognitive impairment
- 1. Subjective memory complaints
- 2. Objective cognitive deficits on testing
- 3. Functioning OK
82Vascular dementia - onset
- Q. Relative to age, what is the incidence of the
onset of vascular dementia?
83Vascular dementia - onset
- Ans. Gradually increases with age, so forms an
increased percentage of those with neurocognitive
disorders with age, such as those gt85. More
common in men.
84Lewy body disease
- Q. Lewy body disease differs in clinical
presentation from Alzheimers in what ways?
85Lewy body disease
- Ans. Differs
- -- early and more prominent visual hallucinations
- -- early and more prominent Parkinsonian features
leading to falls - -- more rapid decline
86Lewy body disease - meds
- Q. When you decide to prescribe antipsychotic
medications to someone with Lewy body disease
has, what prominent signs are your concern?
87Lewy body disease - meds
- Ans. Very sensitive to extrapyramidal signs.
88Frontotemporal dementia
- Q. Characteristics of frontotemporal dementia in
comparison to Alzheimers?
89Frontotemporal dementia
- Ans.
- -- personality change early
- -- apathy early
- -- emotional blunting early
- -- disinhibition early
- -- language abnormalities early
- -- memory problems late
- -- apraxia late
- the examiner may use Picks disease for this
entity - Hard to remember all 7 items, but recalling that
memory is relatively late may get you the correct
answer.
90Frontotemporal dementia - onset
91Frontotemporal dementia - onset
- Ans. Onset tends to be between 50 and 60.
92Huntingtons disease - gene
- Q. Genetic aspect of Huntingtons?
93Huntingtons - genes
94Huntingtons - pathology
- Q. Pathology of Huntingtons?
95Huntingtons - pathology
- Ans. While there is damage to many subcortical
structures, the answer they are probably looking
for is basal ganglia.
96Creutzfeldt-Jakob disease - etiology
- Q. What two etiologies are seen in this disease?
97Creutzfeldt-Jakob disease - etiology
- Ans.
- -- slow virus
- OR
- -- a prion proteinaceous infectious particle
98Tardive Diskinesia risks
- Q. Relatively to age, gender, and dementia, what
are TD risks when using antipsychotics?
99TD risks
- Ans. Relative to use of antipsychotics, increased
risk - 1. in women,
- 2. increased risk in the elderly and
- 3. increased in those with dementia
100delirium
- Q. What meds used in psychiatry are associated
with delirium when used with people with
Alzheimers?
101delirium
- Ans. Virtually all Practice Guideline
102Exercise
- Q. Role of exercise in pts with Alzheimers?
103Exercise
- Ans. Reduces depression in addition to other
health benefits.
104MMSE moderate level
- Q. Moderate level of dementia is associated with
what MMSE score?
105MMSE moderate level
106Alzheimers Neuropathology?
107Ans. Alzheimers Neuropathology
- 1 Flattened cortical sulci
- 2 Enlarged cerebral ventricles
- 3 Senile plaques
- 4 Neurofibrillary tangles
- 5 Neuronal loss, especially in the cortex and
hippocampus - 6 Granulovascular degeneration in the neurons
108Also seen in?
- Neuropathology of Alzheimers also seen in?
109Ans. Also seen in.
- 1 Downs
- 2 Dementia pugilistica
- 3 Parkinson-dementia complex of Guam
- 4 Hallervoren-Spatz Disease
- 5 Familial Multiple System Taupathy
- 6 Normals as they age
110Senile PlaquesComposed of?
111Senile PlaquesComposed of
112Neurotransmitters Often Implicated in
Alzheimers?
113Neurotransmitters OftenImplicated in Alheimers
- 1 Acetylcholine, hypoactive
- 2 Norepinephrine, hypoactive
114Cholinergic Antagonists?
- Two cholinergic antagonists that impair cognitive
ability?
115Cholinergic Antagonists
- 1 Scopolamine
- 2 Atropine
- Not complete, but likely to reach questions.
116Cholinergic Agonists?
- Name of cholinergic agonists that would enhance
cognition?
117Cholinergic Agonist
118Vascular Dementia Seen In?
119Vascular DementiaIs Seen In
120Binswangers Disease?
- Pathology of Binswangers Disease?
121Binswangers Disease
- Many small infarcts of the white matter that
spares the cortical region.
122Picks DiseasePathology?
123Picks DiseasePathology
- Also called Frontotemporal Dementia.
- Atrophy in the frontotemporal region where
neuronal loss, gliosis, and masses of
cytoskeletal elements are most present.
124What isKluver-Bucy Syndrome?
125Kluver-Bucy Syndrome
- 1 Hypersexuality
- 2 Placidity
- 3 Hyperorality
126Kluver-BucySyndrome Caused By?
127Kluver-Bucy Syndrome Caused By
- Damage to both medial temporal lobes.
128Bradyphrenia?
129Bradyphrenia
- Bradyphrenia is a neurological term referring to
the slowness of thought common to many disorders
of the brain. - Disorders characterized by bradyphrenia include
Parkinson's disease and forms of schizophrenia.
Bradyphrenia can also be a side effect of
psychiatric medications
130Sundowner Syndrome?
- 1 Clinical picture?
- 2 Causes?
131Sundowner Syndrome
- Clinical picture confusion and ataxia.
- Causes in demented patients when external
stimuli, light or interpersonal cues are
diminished.
132Step-wise Cognitive Deterioration?
133Step-wise Deterioration
- Seen in vascular dementia
134Alcohol withdrawal?
- Manifestations?
- Treatment?
135Alcohol withdrawalManifestations
- Irritability, nausea, vomiting, insomnia,
malaise, autonomic hyperactivity, shakiness
136Alcohol withdrawaltreatment
- Fluids, sedate with benzodiazepines, 100 mg
thiamine IM
137Idiosyncratic AlcoholIntoxication?
- 1 manifestation?
- 2 treatment?
138Idiosyncratic AlcoholIntoxication, Manifestation
- Marked aggressive and assaultiveness.
139Idiosyncratic Alcohol Intoxication - treatment
140Q. Alzheimers Diagnostic Markers
141Ans. Alzheimers Diagnositc Markers
- 1 cortical atrophy
- 2 amyloid-predominant neuritic plaques
- 3 tau-predominant neurofibrillary tangles
142Q. Markedly Diminishedin Alzheimers
143Ans. Markedly Diminishedin Alzheimers
- Choline acetyltransferase
- Acetylcholine
144Q. If need a benzodiazepinein treating
Alzheimers
145Ans. If needing a benzodiazepine in treating
Alzheimers
- Go with short acting, lorazepam or oxazepam
146Q. If Needing to use an antipsychotic?
147Q. If needing to use an antipsychotic
- Ans. Select with low anticholinergic activity
148Q. Pathology ofParkinsonians Disease?
149Ans. Pathology of Parkinsonians Disease
- Pathology is especially seen in substantia nigra
150Q. Parkinsons Halluncinations?
151Ans. Parkinsons Hallucinations
152Q. Head TraumaPhysical Findings
153Ans. Head TraumaPhysical Findings
- Ans.
- Blood behind tympanic membrane
- Subconjunctival ecchymosis raccoon eye sign
- Pupillary abnormalities
154Q. Wilsons genetic finding?
155Ans. Wilsons Genetic Finding
156Q. Chronic Traumatic Encephalopathy signs?
157Ans. Chronic Traumatic Encephalopathy - signs
- 1 Dysarthric speech
- 2 Emotional liability
- 3 Slow thinking
- 4 Impulsivity
158Q. Compareas to cognitive severity
- Amyloid-predominant neuritic plaques?
- Tau-predominant neurofibrillary tangles?
159Ans. Compare as toSeverity
- The plaques are more a sign of severity than the
tangles
160Q. Apolipoprotein?
161Ans. Apolipoprotein
- Risk factor for Alzheimers but neither necessary
or sufficient factor.
162Q. Frontotemporal Neurocognitive Disorder
- Pathology?
- Name two types and associated pathology.
163Ans. Frontotemporal Neurocognitive Disorder
- Behavioral-variant has both frontal lobes and
anterior temporal lobes are atrophied - Semantic language-variant has temporal lobe
atrophy at the middle, inferior, and anterior
parts of that lobe
164Q. Wing-beating tremor?
165Ans. Wing-beating tremor,Seen In
166Q. Lewy BodyPathology?
167Ans. Lewy Body
- The underlying neurodegenerative disease is
synucleinopathy due to alpha-synuclein misfolding
and aggregation.
168Q. Tramantic Brain Injury
- Neurological/Mental Signs?
169Ans. TBI
- loss of consciousness
- posttraumatic amnesia
- Disorientation and confusion
- Neurological signs, e.g., seizures
170Q. Creutzfeldt-Jakob
171Ans. Creutzfeldt-Jakob
- One of the prion diseases
172Q. Huntingtons Disease
173Ans. Huntingtons Disease
- Genetic testing for trinucleotide CAG on
chromosome 4.
174Q. Hiranos bodies?
175Ans. Hiranos bodies
- Seen in Alzheimers.
- Hirano bodies are intracellular aggregates of
actin and actin-associated proteins first
observed in neurons (nerve cells) by Asao Hirano
in 1965.1 - Hirano bodies are found in the nerve cells of
individuals afflicted with certain
neurodegenerative disorders, such as Alzheimer's
disease and Creutzfeldt-Jakob disease.2 - Hirano bodies are often described as rod-shaped,
crystal-like, and eosinophilic. - Hirano bodies have been noted as a function of
age without obvious underlying neurodegeration